[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-353989-105":3,"detail-sidebar-cat-0-en-105":80,"doc-detail-353989-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":73,"head_meta":75,"extra_data":77,"updated_unix":79},105,"en","gtpbp2-inactivates-hippo-signaling-to-promote-triple-negative-breast-cancer-cell-malignancy","GTPBP2 inactivates Hippo signaling to promote triple-negative breast cancer cell malignancy","","Breast cancer remains the leading cause of cancer-related mortality among women worldwide, with triple-negative breast cancer (TNBC) showing the poorest prognosis. This study investigates how GTPBP2 influences TNBC proliferation, migration, and invasion, and clarifies underlying mechanisms. GTPBP2 expression was analyzed via breast cancer databases, validated by western blotting, and manipulated using lentiviral infection in TNBC cells. Functional assays and xenograft experiments assessed malignant progression in vitro and in vivo.",{"@graph":14,"@context":72},[15,34,55],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & 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cells via lentiviral infection, and malignant phenotypes were assessed using CCK-8, colony formation, wound-healing, and Transwell invasion assays, with additional validation using xenograft tumors in B-NDG mice.","https://schema.org",{"og:url":32,"og:type":74,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":76,"canonical":32},"index,follow",{"doc_id":78,"site_id":7},353989,1790218070,{"code":4,"msg":81,"data":82},"success",[83,87,91,95,100,105,110,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":84,"show_sort_weight":85,"slug":86},"Story & 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promote triplenegative breast cancer cell malignancy  \nXian Zhao1,3, Wenjing Li1,3, Qinyu Han1, Xingchao Xu1,2, Chuanxin Ren2, Wenfeng Liu1 & Xiangqi Li1􀀍  \nBreast cancer (BC) remains the leading cause of cancer-related mortality among women worldwide, with triple-negative breast cancer (TNBC) exhibiting the poorest prognosis. GTPBP2, a member of the G protein superfamily, has primarily been studied in the context of human genetics, with no reported research on its role in BC. This study aims to explore the effects of GTPBP2 on proliferation, migration, and invasion inTNBC, as well as to elucidate its underlying mechanisms. In this study, GTPBP2 expression was analyzed using multiple breast cancer-related databases. Western blotting was employed to validate the protein expression of GTPBP2 and its potential mechanisms in human breast cancer. Additionally, lentiviral infection was used to alter GTPBP2 expression inTNBC cells, and the effects on cancer cell proliferation, migration, and invasion were assessed in vitro using CCK-8 assays, colony formation assays, wound-healing assays, and Transwell invasion analyses. To further evaluate the role ofGTPBP2 in vivo, xenograft tumors were established in female B-NDG mice to study tumor occurrence and progression. GTPBP2 is significantly upregulated inTNBC tissues and plays a critical role in promoting the malignant progression of breast cancer by positively regulating key pathways associated with tumor growth and metastasis.  \nKeywords GTPBP2, Proliferation, Migration, Invasion  \nBreast cancer is one of the most prevalent malignancies affecting women worldwide1,2, characterized by the uncontrolled growth of cells within breast tissue. Based on the expression status of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), breast cancer is classified into four main subtypes2: Luminal A, Luminal B, HER2-enriched, and triple-negative breast cancer (TNBC) . Among these, TNBC accounts for approximately 10–20% of all breast cancer cases and is distinguished by its poor prognosis and high recurrence rates3. TNBC is an aggressive subtype defined by the lack of expression of ER, PR, and HER2, making it unresponsive to targeted hormonal or HER2-directed therapies. This absence of key therapeutic targets has rendered TNBC treatment particularly challenging4. Historically, treatment options for TNBC have primarily involved chemotherapy and surgery. However, with advances in medicine and biotechnology, modern approaches now include targeted therapies and immunotherapies5,6. These innovations have marked a shift toward more precise and individualized treatment strategies. Given TNBC’s aggressive nature, poor clinical outcomes, and limited treatment options, there is an urgent need for biomarker discovery and the development of novel therapeutic strategies to improve patient survival and overall outcomes.  \nGTP-binding protein 2 (GTPBP2) is a member of the large GTPase family, which acts as molecular switches to regulate various cellular processes by cycling between an active, GTP-bound state and an inactive, GDPbound state7. GTPBP2 is believed to play a critical role in ensuring translational fidelity and may be involved in resolving stalled ribosomes during protein synthesis. Additionally, it has been implicated in the regulation of RNA metabolism, particularly during the translation process8. The gene encoding GTPBP2 is located on chromosome 6 in humans, and its expression has been observed in a wide range of tissues, including the brain9, underscoring its importance in maintaining cellular homeostasis. Recent studies suggest that mutations in the GTPBP2 gene may contribute to neurological disorders, including neurodegenerative diseases10. Despite these  \n1Department of Breast Center, The Second Affiliated Hospital of Shandong, Fi","cbCaieP2rFj6LqxC","https://ap.wps.com/l/cbCaieP2rFj6LqxC","pdf",2244628,12,"English","# Background and Rationale\n## Breast cancer subtypes and TNBC challenges\n## GTPBP2 and potential cellular functions\n## Hippo signaling pathway overview\n# Study Objectives\n## Expression, prognosis, and clinical associations\n# Methods and Experimental Approach\n## Database analysis and western blot validation\n## Lentiviral modulation and in vitro assays\n## Xenograft tumor model in vivo","[{\"question\":\"What is the main research question of this study?\",\"answer\":\"The study examines how GTPBP2 affects TNBC malignant behaviors such as proliferation, migration, and invasion, and what mechanisms may be involved.\"},{\"question\":\"How was GTPBP2 expression studied and validated?\",\"answer\":\"GTPBP2 expression was analyzed using multiple breast cancer-related databases and validated at the protein level using western blotting.\"},{\"question\":\"What experimental systems were used to test the effects of GTPBP2 in TNBC?\",\"answer\":\"GTPBP2 was altered in TNBC cells via lentiviral infection, and malignant phenotypes were assessed using CCK-8, colony formation, wound-healing, and Transwell invasion assays, with additional validation using xenograft tumors in B-NDG mice.\"}]","GTPBP2 inactivates Hippo signaling to promote triple-negative breast cancer cell malignancy | PDF",1790108365]